Repair of complete atrioventricular canal: 1975-1985.
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Biomedical subjects
Publications and source records attributed to A Mazzucco.
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The risk of surgical treatment of tetralogy of Fallot was analyzed with multivariate statistical techniques in a recent surgical series (1975-1983) of 159 corrected and 59 palliated patients. The overall mortality of correction was 12.6% and that of palliation was 15.3%. The significant and independent risk factors that increased the mortality of palliation were the use of a shunt other than the Blalock or its modifications (mostly Waterston) (P = 0.01), and very young age (P = 0.02). Risk factors that increased the mortality of correction were high left over right ventricular pressure ratio (P-RV/LV) (P = 0.02), persistent patency of the arterial duct (P = 0.02), other major associated lesions (P = 0.02), and the use of a transannular patch (P = 0.04). Cardioplegia significantly decreased the risk (P = 0.03). With present techniques, correction can be performed in favorable cases with a mortality approaching zero. Staged procedures neutralized the age related risk of correction, but Blalock shunts carried a mortality rate ranging from 9.5% at 1 month to 1.7% at 12 months of age. This was due to the lack of prostaglandins along with technical faults. Predicted two-stage mortality rates ranged in infants (less than 12 months) from 6.2 to 16% and compared favorably with our observed 27% mortality of primary correction. Our results show that the transannular patch becomes a fully expressed risk only in those patients with restrictive pulmonary arteries or isolated branch stenosis. This is because it decreases the force the right ventricle can generate in maintaining the cardiac output. The chances of survival, when compared with those of patients without transannular patch, are significantly less when the P-RV/LV is between 0.6 and 1.0. We therefore discuss the measures to decrease or neutralize this risk related to insertion of a transannular patch. Among the associated lesions, we discuss briefly the potential for residual right outflow tract stenosis, anomalous origin of the left anterior descending coronary artery and anomalous muscle bundle of the right ventricle.
Disc immobilization by prolapsed sutures is a rare but potential risk after prosthetic heart valve replacement. We present here a simple technical modification used during prosthetic valve insertion, which can prevent the occurrence of such a complication.
From 1977 to 1983, 32 consecutive patients, ranging in age from 15 days to 24 years, underwent operations for double-outlet right ventricle. Twenty patients had a palliative operation either to increase (12 cases) or to reduce (eight cases) pulmonary blood flow: Ten of them have subsequently undergone total repair, and in another six correction was delayed because of possible incremental operative risk factors, such as multiple ventricular septal defects or the need for an extracardiac conduit. Four patients with multiple, complex associated intracardiac anomalies are currently considered to have uncorrectable defects. A total of 22 patients underwent correction either primarily (12) or after palliation (10). Intraventricular tunneling was performed in 16 patients with a subaortic ventricular septal defect and in one with a doubly committed ventricular septal defect. Seven of these had pulmonary stenosis and five had reconstruction of the right ventricular outflow by means of a patch (three) or a conduit (two); among this group, five also had enlargement of the ventricular septal defect. In three patients with a subpulmonary defect and in one with a remote ventricular septal defect, all of them without pulmonary stenosis, total repair was achieved by a Senning, a Mustard, or an arterial switch operation. Finally, the only patient with atrioventricular discordance and pulmonary stenosis had insertion of a left ventricle-pulmonary artery conduit. No operative deaths were observed after palliation, but one patient died of intrapulmonary hemorrhage after total repair (4.5%). Major postoperative complications included detachment of the ventricular septal defect patch in one patient and late progression of pulmonary vascular obstructive disease in another. No late deaths have been recorded. Surgical repair of double-outlet right ventricle can be accomplished with gratifying early and late results, the risk of operative death being below 5%. The outcome in patients with subaortic ventricular septal defect appears particularly favorable, despite the extensive intracardiac procedures required for total correction. An early intervention is recommended to prevent development of pulmonary vascular obstructive disease and to avoid massive cardiac hypertrophy and fibrosis, which may cause late rhythm disturbances and impede the intracardiac repair.
Results of reoperation for primary tissue failure of porcine bioprostheses were evaluated in 574 patients discharged from the hospital from 1970 to 1981. A total of 413 had undergone isolated mitral valve replacement and 161 isolated aortic valve replacement. Through March, 1984, 88 patients (15%) had required reoperation: 59 had undergone mitral and 29, aortic valve replacement. Primary tissue failure was the main cause of bioprosthetic dysfunction; it occurred in 64 patients (46 mitral and 18 aortic) at a mean postoperative interval of 93 +/- 4 months (range 34 to 158). During the same period, 11 patients required reoperation for bioprosthetic endocarditis, 11 for paravalvular leak, and two for thrombosis. These patients are not included in this review. Reoperation for primary tissue failure was performed after a mean interval of 72 +/- 6 months (range 38 to 158) for patients with aortic bioprostheses and after 101 +/- 5 months (range 34 to 153) for those with mitral bioprostheses (p less than 0.05). Overall mortality at reoperation was 12.5%: 11% for the mitral group and 16% for the aortic group. In 62 patients (45 mitral and 17 aortic) primary tissue failure was caused by calcification of the cusps, associated with severe fibrous tissue overgrowth in seven. Bioprosthetic failure was caused by an intracuspal hematoma in one patient with mitral valve replacement and by lipid infiltration of the cusps in one patient with aortic valve replacement. Actuarial freedom from bioprosthetic primary tissue failure at 12 years is 61% +/- 5% for the mitral group and 69% +/- 7% for the aortic group. On the basis of our long-term follow-up of patients after mitral or aortic replacement with a porcine bioprosthesis, we conclude: primary tissue failure is the most frequent indication for reoperation in patients with a porcine bioprosthesis; calcification of the cusp tissue is the leading cause of primary tissue failure; reoperation for primary tissue failure may be a major concern, although mortality for elective cases is low; and the limited durability of porcine bioprostheses suggests their use be restricted to selected patients.
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Sixty-seven glutaraldehyde-processed porcine bioprostheses (PBs), recovered at autopsy or reoperation from 65 patients, were evaluated by roentgenologic and pathologic examination. Seven patients with 8 PBs were younger than 20 years of age. The time interval of function was 2 to 138 months (average 62). Pathologically, 53 explants had signs of intrinsic dysfunction, which was ascribed to calcification in 36 (68%). By x-ray examination, calcific deposits were found in 55 of 67 PBs (82%). The mean duration of function was 70 +/- 32 months in calcified PBs vs 27 +/- 18 months in noncalcified PBs (p less than 0.001). All 26 PBs that had been in place for longer than 6 years were calcified. In 45 PBs the Ca++ deposits were considered severe (mean time of function 76 +/- 32 months) and mild in 10 (mean time of function 44 +/- 22 months) (p less than 0.005). The Ca++ deposits were located at the commissures in 54 PBs (98%), at the body of cusps in 41 (75%), at the free margin in 37 (67%) and at the aortic wall in 37 (67%). When mild, Ca++ deposits involved the commissures in 90% of cases, the body of cusps in 30% and the free margin only in 10%. Forty-seven calcified PBs were mounted on a flexible stent, and 8 had a rigid stent, with an average time of function of 63 +/- 28 and 113 +/- 18 months, respectively (p less than 0.00001). Ca++ dysfunction occurred earlier in the aortic than in the mitral position (59 +/- 19 vs 86 +/- 35 months, p less than 0.05). All the PBs explanted from young patients and 47 of 59 PBs removed from adult patients were calcified, with an average time of function of 50 +/- 21 vs 73 +/- 33 months, respectively (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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Up to the end of 1982, reoperation for dehiscence of an aortic prosthesis was necessary in 5% of patients operated on for primary aortic valve replacement in the previous decade at the University of Padova Cardiac Surgery Center. This complication occurred early (median time to diagnosis 4 months) and was associated with an elevated 30-day operative mortality (27%, 70% CL 19-37%). This is probably (P = 0.09) related to preoperative heart failure. The follow-up of the traced surviving patients (92%) indicates a continuing poor prognosis with a 6-year survival rate of only 13.5% (70% CL 5.0-30%). All the events were cardiac related and directly or indirectly connected with the persistence or recurrence of dehiscence that was observed in 72% of the cases. In the face of these results, a retrospective study has been performed to identify, on the basis of the available data, the subsets of patients more prone to develop this complication. Our results suggest that a significant increased risk (P less than 0.001) can be identified in patients presenting with bacterial endocarditis (12.2% rate), in patients with concomitant aneurysm of the ascending aorta (10.9%) and in patients with degenerative regurgitation or severe calcifications of their native valve, with rates of 7.0 and 6.0 respectively. In these situations particular care is required to avoid undue stress on the annular tissue. We also suggest the use of buttressed interrupted sutures.
Four hundred seventy-six patients underwent isolated mitral valve replacement (MVR) with the glutaraldehyde-preserved porcine Hancock bioprosthesis from March, 1970, through December, 1981. There were 312 female and 164 male patients ranging in age at operation from 9 to 68 years (average, 53 years). Associated surgical procedures were performed in 35 patients. Hospital mortality was 13%, the main cause of death being low-output syndrome. The survivors were followed from 1.6 to 13.2 years (mean, 5.2 years). Cumulative duration of follow-up is 2,180 patient-years and is 97% complete. Overall late mortality is 3.1 +/- 0.3% per patient-year, and actuarial survival is 73.8 +/- 3.4% at 13 years. Embolic accidents occurred in 45 patients and were fatal in 13; the linearized incidence of postoperative systemic thromboemboli is 2.1 +/- 0.3% per patient-year. Reoperation was necessary in 49 patients: in 4 because of valve endocarditis, with 3 deaths; in 6 because of perivalvular leak, with no deaths; in 2 because of left atrial thrombosis; and in 37 because of valve dysfunction due to primary tissue failure, caused mainly by calcific degeneration of the tissue, with 5 operative deaths. Actuarial freedom from primary tissue failure is 58 +/- 6.6% at 13 years. Extended follow-up after MVR with the Hancock bioprosthesis confirms the satisfactory performance and low thrombogenicity of this device up to 13 years after operation.(ABSTRACT TRUNCATED AT 250 WORDS)
The possible determinants of a fatal outcome following surgical repair of the tetralogy of Fallot were analyzed by postmortem examination in 14 cases. Only one patient died late in the postoperative period, due to patch detachment; the others died shortly after undergoing surgery. Death could not be explained in three cases. In three patients with perimembranous ventricular septal defects, complete atrioventricular block occurred as a consequence of traumatic disruption of the branching bundle. In four cases residual stenosis of the pulmonary outflow tract was shown; in one of these cases adequate relief of obstruction had been prevented by a large conal coronary artery. A residual mitral cleft was found in one patient. Death was not related to the cardiac conditions in two cases; one of these patients died of brain apoplexy and the other of tracheal hemorrhage. These findings stress the need for accurate preoperative diagnosis and precise knowledge of the surgical anatomy of this malformation.
From January 1968 to July 1983, 38 patients with an intracardiac myxoma underwent surgical excision of the tumor at our Institution. There were 15 males and 23 females, ranging in age from 17 to 68 years (mean 47.7). In all but 2 patients, the presence of an intracardiac myxoma was documented preoperatively by angiographic and/or echocardiographic study. The first 2 patients of this series were referred with the diagnosis of mitral stenosis, and the myxoma was an unexpected surgical finding. In 32 cases (84.2%) the myxoma was located in the left atrium, in 4 (10.5%) in the right atrium and in 2 (5.3%) in the right ventricle. Surgery was performed on an emergency basis in 36 patients. Two patients (5.2%) both with a left atrial myxoma, died after surgery: one died intraoperatively of hemorrhage and the other after one month of bowel infarction. Follow-up of the 36 survivors ranges from 3 months to 14.5 years (average 5.2 yr); all were controlled by means of clinical and echocardiographic investigations, and no evidence of tumor recurrence was detected. Surgery for intracardiac myxoma, which should be undertaken on an emergency basis, carries a low operative risk; excision of the tumor appears to be curative with no recurrences at long-term follow-up; non-invasive tools are of the utmost importance in both the preoperative assessment and follow-up of these patients.
Clinical, vectorcardiographic, and echocardiographic data from two siblings with atrial septal defects and dysplasia of the mitral and tricuspid valves are reported. Vectorcardiograms showed that both siblings had abnormal ventricular activation with initial electrical forces directed posteriorly. One sibling died after surgery, and necropsy showed incomplete differentiation of the leaflets and tensor apparatus producing anomalies resembling "mitral arcade." Serial histological examination of the conducting tissue showed that the atrioventricular node was located on the left side of the atrial septum, that the central fibrous body and the membranous septum were hypoplastic, and that an accessory nodoventricular pathway originating in the compact node joined the left side of the ventricular septum. This accessory pathway was probably the cause of the unusual ventricular activation. Dysplasia of the mitral and tricuspid valves together with hypoplasia of the central fibrous body and the presence of accessory pathways are probably part of a malformative complex caused by incomplete differentiation of both the cardiac atrioventricular valves and the junctional area.
Between 1 January 1975 and 31 December 1982, 111 patients with atrioventricular septal defect underwent surgical repair. Of these, 43 had the complete, 11 the intermediate, and 57 the partial form. The postoperative mortality rate was 37%, 9%, and 6% respectively. To determine which factors were independently responsible for the operative risk multivariate analysis of the surgical mortality was applied simultaneously to all three forms of the malformation. The form of defect, although strongly influencing the natural history and clinical presentation, was not by itself an operative risk factor. The risk was related primarily to failure to obtain a well functioning atrioventricular valve, to the presence of left ventricular dominance, to the degree of pulmonary vascular resistance, and, finally, to the technique of reconstructing a two leaflet left atrioventricular valve. The small size of the patient was also a significant incremental risk factor, but if the other factors were not unfavorable good results could be achieved in small infants with mortality rates less than 10%. Multivariate analysis showed that severe postoperative left atrioventricular valve malfunction was related to the technique used to reconstruct a "normal" two leaflet left atrioventricular valve. These findings support the policy of reconstructing the left atrioventricular valve as a three leaflet valve. Nevertheless, the implicit beneficial effect of this technique has not as yet proved to be statistically significant.
Five patients, who developed sternal wound infection following open heart surgery and in whom the standard methods of management of this complication had been unsuccessful, were treated with an autogenous vaccine. Complete healing of the sternal wound was obtained in 4 of them, while in one, who had an associated mediastinitis, a slow recovery with persistence of a sternal fistula occurred. The results of this preliminary experience indicate that the use of an autogenous vaccine might be regarded as an alternative method of treatment of sternal infections in selected patients.
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Between January 1970 and December 1981, a total of 21 reoperations for periprosthetic leak were performed on 20 patients out of 999 with previously implanted prosthetic mitral valves. In most of them reoperations were performed within the first year, since the initial procedure and the leading indications were intractable congestive heart failure or infection of the mitral prosthesis. The mortality rate was 30% and was related to the preoperative cardiac functional status. The preoperative variables significantly related to an increased incidence of dehiscence of the mitral prosthesis necessitating reoperation were a degenerative disease (P = 0.016) or an infective endocarditis (P = 0.0006) of the native valve, both causing mitral regurgitation. Rheumatic disease, type of prosthesis, supra- or subannular insertion, age of the patient, and operative year, were not significant, neither were calcifications that are probably neutralized by the routine use of special surgical techniques. It is suggested that the use of techniques specifically designed to eliminate periprosthetic leak in patients affected by mitral regurgitation due to degenerative or infective disease of the native valve, might lead to a further reduction of reoperations for this complication.